ArticleCancer medicine2018
The regulatory role of APE1 in epithelial-to-mesenchymal transition and in determining EGFR-TKI responsiveness in non-small-cell lung cancer.
Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- ALK Knock-In Reporter Reveals APE1 as a Negative Regulator ofInternational journal of molecular sciences · 2026Article
- Synergistic Reduction of Breast Cancer Cell Viability and Aggressiveness Through Dual Inhibition of APE1 Redox Function and STAT3 Signaling.Cell biology international · 2025Article
- Isoliensinine exerts antitumor effects in lung adenocarcinoma by inhibiting APEX1-driven ROS production.Frontiers in pharmacology · 2025Article
- Apurinic/Apyrimidinic Endodeoxyribonuclease 1 modulates RNA G-quadruplex folding of miR-92b and controls its expression in cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Overcoming EGFR-TKI resistance by targeting the tumor microenvironment.Chinese medical journal pulmonary and critical care medicine · 2024Review
- Selective anti-tumor activity of glutathione-responsive abasic site trapping agent in anaplastic thyroid carcinoma.BMC cancer · 2024Article
- New Ref-1/APE1 targeted inhibitors demonstrating improved potency for clinical applications in multiple cancer types.Pharmacological research · 2024Article
- Clinical translation for targeting DNA damage repair in non-small cell lung cancer: a review.Translational lung cancer research · 2024Review
- The APE1/REF-1 and the hallmarks of cancer.Molecular biology reports · 2024Review
- Article
- APE-1/Ref-1 Inhibition Blocks Malignant Pleural Mesothelioma Cell Proliferation and Migration: Crosstalk between Oxidative Stress and Epithelial Mesenchymal Transition (EMT) in Driving Carcinogenesis and Metastasis.International journal of molecular sciences · 2023Article
- Levels of APE1 Repair Gene and CLEC4M in Lung Cancer Patients Receiving Cisplatin Chemotherapy.Archives of Razi Institute · 2023Article
- The Role of DNA Damage and Repair in Idiopathic Pulmonary Fibrosis.Antioxidants (Basel, Switzerland) · 2022Review
- APE1 controls DICER1 expression in NSCLC through miR-33a and miR-130b.Cellular and molecular life sciences : CMLS · 2022Article
- SOX2 knockdown with siRNA reverses cisplatin resistance in NSCLC by regulating APE1 signaling.Medical oncology (Northwood, London, England) · 2022Article
- Inhibiting the redox function of APE1 suppresses cervical cancer metastasis via disengagement of ZEB1 from E-cadherin in EMT.Journal of experimental & clinical cancer research : CR · 2021Article
- Lentivirus-mediated silencing of CNTN1 enhances gefitinib sensitivity by reversing epithelial-mesenchymal transition in lung adenocarcinoma A549 cells.Oncology letters · 2021Article
- Exosome-derived miR-210 involved in resistance to osimertinib and epithelial-mesenchymal transition in EGFR mutant non-small cell lung cancer cells.Thoracic cancer · 2021Article
- Small-molecule inhibition of APE1 induces apoptosis, pyroptosis, and necroptosis in non-small cell lung cancer.Cell death & disease · 2021Article
- Inhibition of APE1/Ref-1 Redox Signaling Alleviates Intestinal Dysfunction and Damage to Myenteric Neurons in a Mouse Model of Spontaneous Chronic Colitis.Inflammatory bowel diseases · 2021Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpithelial-to-mesenchymal transition (EMT) plays a pivotal role in resistance to EGFR tyrosine kinase inhibitors (TKIs) in non-small-cell lung cancer (NSCLC). Our previous study revealed that in osteosarcoma, human apurinic/apyrimidinic endonuclease 1 (APE1) regulates transforming growth factor-β (TGF-β), an important player in EMT. We therefore hypothesized a link between APE1 and EGFR-TKI responsiveness in NSCLC.
methodsThe protein levels of APE1 were analyzed in tumors of NSCLC patients receiving EGFR-TKI treatment. The correlation between APE1 expression and progression-free survival (PFS), overall survival (OS), or response rate were analyzed. The impact of APE1 on the response to EGFR-TKIs was measured by exogenous manipulation of APE1 in EGFR-TKI-sensitive and EGFR-TKI-resistant cells.
resultsWe indicate that low expression of APE1 in tumors is associated with a significantly longer PFS (20.8 months vs 8.4 months, P = 0.008) and a preferential OS (39.0 months vs 17.0 months, P = 0.001), with no difference in initial response rate to EGFR-TKIs. We observed that APE1 protein level was significantly increased in EGFR-TKI-resistant cells and was associated with downregulated E-cadherin and upregulated vimentin. The EMT phenotype, as well as the levels of TGF-β, was suppressed in APE1 knockdown HCC827/IR and PC-9/ER cells, while the EMT phenotype was promoted in APE1-overexpressed HCC827 and PC-9 cells. Furthermore, a specific APE1 redox inhibitor (ie, E3330) effectively reversed the EMT phenotype and further sensitized the cells to EGFR-TKIs.
conclusionThis study revealed a significant role of APE1 in EGFR-TKI resistance via novel regulatory effects on the EMT phenotype in NSCLC.
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